Impact Factor 4.137 | CiteScore 4.28
More on impact ›

Mini Review ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Oncol. | doi: 10.3389/fonc.2019.00834

Chemoresistance Mediated by ceRNA Networks Associated with the PVT1 Locus

  • 1Hunter College (CUNY), United States

Competitive endogenous RNA (ceRNA) networks have emerged as critical regulators of carcinogenesis. Their activity is mediated by various non-coding RNAs (ncRNAs), including long non-coding RNAs and microRNAs, which competitively bind to targets, thereby modulating gene expression and activity of proteins. Of particular interest, ncRNAs encoded by the 8q24 chromosomal region are associated with the development and progression of several human cancers, most prominently lncPVT1. Chemoresistance presents a significant obstacle in the treatment of cancer and is associated with dysregulation of normal cell processes, including abnormal proliferation, differentiation, and epithelial-mesenchymal transition. CeRNA networks have been shown to regulate these processes via both direct sponging/repression and epigenetic mechanisms. Here we present a review of recent literature examining the contribution of ncRNAs encoded by the PVT1 locus and their associated ceRNA networks to the development of resistance to common chemotherapeutic agents used to treat human cancers.

Keywords: PVT1, lncRNA, ceRNA, miRNA, chemoresistance, Carcinogenesis, 8q24, Cancer

Received: 22 May 2019; Accepted: 13 Aug 2019.

Edited by:

Rengyun Liu, School of Medicine, Johns Hopkins University, United States

Reviewed by:

Jisha Antony, University of Otago, New Zealand
Konrad Huppi, National Cancer Institute (NCI), United States  

Copyright: © 2019 Ogunwobi and Kumar. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Olorunseun O. Ogunwobi, Hunter College (CUNY), New York City, United States, ogunwobi@genectr.hunter.cuny.edu